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Quantitative Imaging of Lineage-specific Toll-like Receptor-mediated Signaling in Monocytes and Dendritic Cells from Small Samples of Human Blood
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Effect of aging and oral tolerance on dendritic cell function.

P U Simioni1, L G R Fernandes, D L Gabriel

  • 1Departamento de Microbiologia e Imunologia, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, Brasil.

Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas
|December 8, 2009
PubMed
Summary

Aging does not prevent oral tolerance induction in mice but impairs dendritic cell function. Dendritic cells from older mice show reduced co-stimulatory molecule expression, impacting T cell responses.

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Area of Science:

  • Immunology
  • Aging Research
  • Allergy and Immunology

Background:

  • Oral tolerance, the immune system's unresponsiveness to ingested antigens, is crucial for preventing allergies.
  • Dendritic cells (DCs) play a key role in initiating immune responses, including those related to oral tolerance.
  • The impact of aging on DC function and oral tolerance is not fully understood.

Purpose of the Study:

  • To investigate how aging affects the induction and maintenance of oral tolerance.
  • To determine the influence of aging on dendritic cell (DC) function in the context of oral tolerance.
  • To examine the expression of co-stimulatory molecules on DCs from aged and tolerized mice.

Main Methods:

  • Oral tolerance was induced in BALB/c mice of various ages (8-80 weeks) using dietary antigens.
  • Dendritic cells (DCs) were isolated from tolerized, immunized, and control mice.
  • DC function was assessed by their ability to induce naive T cell proliferation and cytokine secretion (IFN-γ, IL-4, IL-10, TGF-β).
  • Expression of the CD86 co-stimulatory marker on DCs was quantified.

Main Results:

  • Oral tolerance was successfully induced in mice of all ages, though antibody levels declined with age.
  • DCs from young to middle-aged tolerized mice showed reduced capacity to stimulate T cell proliferation and cytokine production compared to immunized mice.
  • DCs from aged (60-80 weeks) tolerized and immunized mice were similarly ineffective in inducing T cell responses.
  • A significant reduction in CD86 expression was observed on DCs from both aged and tolerized mice.

Conclusions:

  • Aging does not impede the establishment of oral tolerance in BALB/c mice.
  • The aging process significantly impairs dendritic cell function, likely due to decreased CD86 expression.
  • Reduced DC function in aged mice may compromise their ability to mount effective T cell-mediated immune responses.